Identification and characterization of a putative lipopolysaccharide-induced TNF-alpha factor (LITAF) homolog from Singapore grouper iridovirus.

Lipopolysaccharide-induced TNF-alpha factor (LITAF), a transcription factor, can regulate tumor necrosis factor alpha (TNF-alpha) transcription. Here, a novel LITAF homolog encoded by Singapore grouper iridovirus (SGIV LITAF) was identified and characterized. The putative SGIV LITAF encoded a protein of 104 amino acids (aa) with a predicted molecular mass of 11.6 kDa. Reverse transcription-PCR (RT-PCR) and Western blot analyses of SGIV-infected cells revealed that SGIV LITAF was an early viral gene. Subcellular localization and immunofluorescence assay revealed that SGIV LITAF expression was distributed predominantly in the cytoplasm, associated with mitochondria. Overexpression of SGIV LITAF induced apoptosis, as shown by increased apoptotic bodies, depolarization of mitochondrial membrane potential (DeltaPsi(m)) and activation of caspase-3. Furthermore, NF-kappaB and NFAT activities were increased in cells expressing SGIV LITAF. This is the first report of the identification and characterization of a viral LITAF homolog involved in virus-host interaction.